Acetaminophen (paracetamol) is a selective cyclooxygenase-2 (COX-2) inhibitor with IC50 of 25.8 μM, It is a widely used antipyretic analgesic[1].

Paracetamol (50 mM) significantly reduces cell viability. But co-treatment with acetaminophen and HV110 can significantly increase cell viability[2].

Paracetamol (250 mg / kg) reduces glutathione levels and glutathione peroxidase activity in mice, and induces mast cell death and hypertrophy in primary mouse liver cells The inhibitor ferrostatin-1 can block this effect. Paracetamol has analgesic and antipyretic effects in animal models.

References:

[1]. Hinz, B, et al. Acetaminophen (paracetamol) is a selective cyclooxygenase-2 inhibitor in man, 2008, 22(2): 383-90.

[2]. Dini M, et al. Lactobacillus fermentum Postbiotic-induced Autophagy as Potential Approach for Treatment ofAcetaminophen Hepatotoxicity. Front Microbiol, 2017, 8: 594.

[3]. L?rincz T, Jemnitz K, Kardon T,?et al. Ferroptosis is Involved in Acetaminophen Induced Cell Death. Pathology & Oncology Research, 2015, 21(4): 1115-1121.